Browsing by Author "Mena, María A."
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- Acute effects of ethanol on brain, plasma and adrenal monoamine concentrations in virgin and pregnant rats and their fetuses .
1986-09-19T15:40:12Z The dose-response relationship in brain. plasma, and adrenal mon()aminc changes after acute oral ethanol administration (I, 2. 4 g./kg body wt) was sl u-licd in virgin rats lo determine whether the response lo the highest dose differed in 21-day pregnant ani11ials. and to assess the potential consequences of ethanol on the neurotransmitlcr systems of their fctusc s. Blood ethanol and acetaldchyde concentrations in blood increased progrcs:;ivcly with the ctha1wl dose in virgin rats, and values in pregnant animals were very similar. Ethan,>! concentration in fetal blood and amniotic Ouid did not differ from that in mother's blood whereas fetal acctaldchydc concentrations were negligible. In a dose-related manner, ethanol decreased brain DA. DOPAC and 5HT ..:cncentrations did not affect those of NA and 5HIAA, or adrenal A and NA concentrations, whereas it enhanced plasma NA levels. Basal levels of monoamincs and their changes after ethanol intake did not differ in pregnant and virgin rats. Monoaminc and metabolite concentrations were much lower in fetal tlian in maternal brains whereas plasma and adrenal catecholamine concentrations were very similar and naternal ethanol intake did not modify these fetal parameters in the fetus. Results are in agreement wi1 h the known similar metabolic response to ethanol in fed pregnant and virgin rats. The lack of fetal monoamine response to maternal ethanol intake may be a consequence of the incapacity of fetal liver to form acetaldchydc and the ability of the placenta to oxidize maternal acctaldehyde which protects the fetus fr,m1 maternal alcohol intake at late gestation.
- Effects of alcohol ingestion in the pregnant rat on daily food intake, offspring growth and metabolic parameters.
1983-09-19T15:40:26Z Daily food intake, fluid consumption, offspring growth and metabolic parameters were studied in rats receiving ethanol in the drinking water before, during and after gestation. 2. Ethanol treatment always reduced daily food, liquid and caloric intake in the rat, except during gestation when total daily caloric intake was greater in rats receiving ethanol than in control animals. The increase in both food and liquid intake during lactation in controls was also observed in alcoholdeprived mothers but was significantly reduced in mothers maintained under alcohol treatment. 3. Offspring from alcohol-treated mothers were retarded in body weight and size compared with controls, the differences becoming greater as the suckling period advanced. 4. The 15 day-old pups from alcohol-treated mothers had reduced glucose and augmented betahydroxybutyrate levels in blood, and markedly reduced liver glycogen concentrations, indicating their acutely denutrited state. 5. In pups from mothers that received alcohol until the 21st day of gestation, body weight and size were normalized at the 15th day but skeletal maturation and liver glycogen concentration were reduced and blood acetoacetate and beta-hydroxybutyrate were augmented as compared with values in pups from control mothers. If these parameters are interrelated, metabolic changes may be used for early diagnosis of fetal alcohol syndrome.
- Monoamine metabolism in rat brain regions following long term alcohol tratment.
1980-09-19T15:39:50Z Female Wistar rats (150-200 g) were treated with ethanol (15 0/o w/v) for 21 days and compared with control rats given water. Ethanol administration produced a reduction of fluid and food consumption and changes in the metabolism of cerebral monoamines. There was an increase in serotonin (5-HT) turnover statistically significant in the striatum, and a decrease in noradrenaline (NA) turnover in ethanol rats as compared to controls. Endogenous NA levels were significantly increased in the diencephalon and dopamine (DA) levels were increased in the striatum. After inhibition of catecholamine synthesis with a-methyltyrosine (a-MT), NA depletion was significantly retarded but no changes in DA depletion were noted. DOPA accumulation after decarboxylation inhibition showed no significant change in any brain region studied.